Epigenetic Regulation of Kidney Development

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular Genetics and Genetic Diseases".

Deadline for manuscript submissions: closed (30 April 2026) | Viewed by 2710

Special Issue Editor


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Guest Editor
Department of Pediatric Nephrology, Tulane University School of Medicine, New Orleans, LA 70112, USA
Interests: epigenetic regulation of kidney development and diseases
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Special Issue Information

Dear Colleagues,

Epigenetic regulation plays a crucial role in kidney development, influencing gene expression patterns without altering the underlying DNA sequence. Advancements in single-cell RNA sequencing (scRNA-seq) and single-cell epigenomics have provided deeper insights into the dynamic epigenetic landscapes during kidney development. These technologies enable the characterization of gene expression and epigenetic modifications at a single-cell resolution, facilitating the identification of distinct cell populations and their developmental trajectories. Such detailed mapping is essential for understanding how epigenetic dysregulation may lead to developmental abnormalities and for developing targeted therapeutic strategies. This Special Issue, entitled "Epigenetic Regulation of Kidney Development", aims to compile recent studies on how epigenetic mechanisms impact kidney formation and associated pathologies.

Dr. Hongbing Liu
Guest Editor

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Keywords

  • epigenetic regulation
  • kidney development
  • gene expression patterns
  • targeted therapeutic strategies
  • epigenetic regulation of kidney development

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Published Papers (2 papers)

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Research

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16 pages, 6247 KB  
Article
Single-Cell Transcriptomic and Metabolic Signatures in Exhausted and Classical Memory B Cells—An Exploratory Analysis in Systemic Lupus Erythematosus and Lupus Nephritis
by Litong Zhu, Taoyan Lin, Lai Yee Cheong, Jason K. H. Sher, Irene Y. L. Yam, Wynn Cheung, Susan Yung, Tak Mao Chan and Desmond Y. H. Yap
Biomedicines 2026, 14(6), 1188; https://doi.org/10.3390/biomedicines14061188 - 25 May 2026
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Abstract
Aim: Disturbances in exhausted and classical memory B cells have been implicated in the pathogenesis of systemic lupus erythematosus (SLE) and lupus nephritis (LN), but the genetic regulation of their homeostasis remains poorly understood. Methods: We analyzed the single-cell RNA-seq data of peripheral [...] Read more.
Aim: Disturbances in exhausted and classical memory B cells have been implicated in the pathogenesis of systemic lupus erythematosus (SLE) and lupus nephritis (LN), but the genetic regulation of their homeostasis remains poorly understood. Methods: We analyzed the single-cell RNA-seq data of peripheral blood mononuclear cells (PBMCs) from the NIH SLE dataset (GSE135779) and another published LN single-cell RNA-seq dataset (dbGAP database accession code phs001457.v1.p1). Overlapping differentially expressed genes (DEGs) in exhausted and classical memory B cells from SLE and LN patients were identified, and their altered expression was validated in B cells obtained from LN patients. GO and KEGG analyses were used to analyze associated pathways. The relationships between exhausted and classical memory B cells and cellular metabolic pathways were also assessed. Results: Three DEGs (IFI44L, XAF1, and MX1) were detected in both exhausted and classical memory B cells, and their increased expression was verified in classical and exhausted memory B cells obtained from LN patients during remission. The protein–protein interaction network of the DEGs suggested that STAT1 showed the highest eigenvector centrality for these DEGs. IFI44L, XAF1 and MX1 were involved in distinct biological processes and immune pathways (especially JAK-STAT). Classical memory B cells showed higher expression of genes involved in sulfur metabolism (SQRDL and TST), amino sugar metabolism (GFPT1 and UAP1), and butanoate metabolism (ACADS and ACAT1), while exhausted B cells exhibited inverse relationships with these metabolic pathways. Conclusions: Altered expression of IFI44L, XAF1 and MX1 is associated with distinct metabolic signatures and immune pathways in exhausted and classical memory B cells in SLE and LN. Full article
(This article belongs to the Special Issue Epigenetic Regulation of Kidney Development)
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Review

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15 pages, 525 KB  
Review
Epigenetic Regulation in Wilms Tumor
by Annabelle Bolitho and Hongbing Liu
Biomedicines 2025, 13(7), 1678; https://doi.org/10.3390/biomedicines13071678 - 9 Jul 2025
Cited by 6 | Viewed by 2209
Abstract
Wilms tumor (nephroblastoma), the most common pediatric renal malignancy, has a complex genetic and epigenetic landscape. While mutations in genes like WT1, CTNNB1, and WTX have been well characterized, accumulating evidence suggests that epigenetic dysregulation plays a pivotal role in WT pathogenesis. This [...] Read more.
Wilms tumor (nephroblastoma), the most common pediatric renal malignancy, has a complex genetic and epigenetic landscape. While mutations in genes like WT1, CTNNB1, and WTX have been well characterized, accumulating evidence suggests that epigenetic dysregulation plays a pivotal role in WT pathogenesis. This review examines the various epigenetic mechanisms implicated in WT, including DNA methylation, histone modifications, chromatin remodeling, and non-coding RNA-mediated regulation. We discuss how epigenetic mechanisms contribute to tumor initiation, progression, and heterogeneity and their implications for improved diagnosis and targeted therapy. We also highlight recent advances in epigenomic profiling, discuss the interplay between epigenetics and developmental gene expression programs, and evaluate potential therapeutic strategies targeting epigenetic regulators. Full article
(This article belongs to the Special Issue Epigenetic Regulation of Kidney Development)
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